Induction of Oxidative Stress in Brain Tissues of Mice after Subchronic Exposure to 2,3,7,8-Tetrachlorodibenzo-p-dioxin

Hassoun, Ezdihar A.; Wilt, Shawn C.; DeVito, Michael J.; Birgelen, Angelique Van; Alsharif, Naser Z.; Birnbaum, Linda S.; Stohs, Sidney J.

doi:10.1006/toxs.1997.2411

Cited by 32 publications

(18 citation statements)

References 37 publications

(35 reference statements)

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“…These findings agree with the data previously obtained in buffalo cows (Spagnuolo et al, 2011), as well as in other laboratory species exposed to either 2,3,7,8 tetrachloro-dibenzo-p-dioxin (Stohs et al, 1984;Hassoun et al, 1998;Slezak et al, 2002) or to DL-PCBs (Lai et al, 2010), and support the hypothesis that the exposure to environmental pollutants, such as dioxins, severely impairs the blood antioxidant defence system. As expected, we found that the lower antioxidant capacity, observed in exposed cows, is associated with a significantly higher extent of oxidative modifications of protein and lipid.…”

Section: Discussionsupporting

confidence: 92%

Analysis of plasma indices of redox homeostasis in dairy cows reared in polluted areas of Piedmont (northern Italy)

Spagnuolo

Cigliano

Nebbia

et al. 2012

Science of The Total Environment

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Steel manufacturing is responsible for the emission of pollutants, including dioxins and transition metals, inducing\ud reactive oxygen species generation and DNA damage. Dioxin pollution represents the major cause of milk and\ud dairy product contamination, in Italy, and is associated with oxidative stress-related processes, that may impair\ud health and performance of cows.We evaluated the effect of exposure to different concentrations of pollutants derived\ud from steel manufacturing on blood redox homeostasis of bovine cows. We analyzed two groups of dairy\ud cows (A, B), reared in two different polluted areas, and a control group of cows bred in an industry free area.\ud The extent of exposure to contaminants was defined by measuring dioxin level in bulk milk samples collected\ud from animals of each farm. This level was lower in milk of group A than in group B. Plasma concentrations of\ud retinol, alpha-tocopherol and ascorbate, the total antioxidant capacity, and the activities of superoxide dismutase\ud and glutathione peroxidase were higher in control group than in exposed groups. In particular, retinol and\ud tocopherol levelswere higher in the groupwith lower milk dioxin level. Plasma titers of protein-bound carbonyls\ud (PC), nitro-tyrosine, and hydroperoxideswere lower in control group than in A or B. Hydroperoxides and PC plasmaconcentrationswere\ud increased in the groupwith higher milk concentration of dioxin. Our results demonstrate\ud that, irrespective of the nature of chemicals inducing oxidativemodifications, the extent of damage to plasmaprotein\ud and lipid, is correlatedwith the concentration of dioxin in milk. So, the characterization of blood redox status\ud might be a useful tool for identifying animals exposed to environmental pollutants. Plasma concentrations of\ud retinol, alpha-tocopherol, PC and hydroperoxides could therefore represent good indices of the extent of animal\ud exposure, as they significantly change in groups with different milk concentrations of dioxi

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Section: Discussionsupporting

confidence: 92%

Analysis of plasma indices of redox homeostasis in dairy cows reared in polluted areas of Piedmont (northern Italy)

Spagnuolo

Cigliano

Nebbia

et al. 2012

Science of The Total Environment

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“…Although oxidative stress does not necessarily result in toxicity, it is an important mechanistic component of many toxicologic processes. In this regard, TCDD-mediated activation of the AHR shifts the cellular redox balance to produce an oxidative stress response (Hassoun et al, 1998;Shertzer et al, 1998;Slezak et al, 2000;Senft et al, 2002a;Senft et al, 2002b). For this reason it has become widely hypothesized that the toxicity induced by TCDD involves an oxidative stress component; an observation that has been reported by several laboratories (Stohs, 1990;Alsharif et al, 1994;Shertzer et al, 1998;Slezak et al, 2000).…”

Section: Tcdd-mediated Perturbation Of Redox Homeostasismentioning

confidence: 98%

Induction of Oxidative Stress Responses by Dioxin and other Ligands of the Aryl Hydrocarbon Receptor

et al. 2005

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ᮀTCDD and other polyhalogenated aromatic hydrocarbon ligands of the aryl hydrocarbon receptor (AHR) have been classically considered as non-genotoxic compounds because they fail to be directly mutagenic in either bacteria or most in vitro assay systems. They do so in spite of having repeatedly been linked to oxidative stress and to mutagenic and carcinogenic outcomes. Oxidative stress, on the other hand, has been used as a marker for the toxicity of dioxin and its congeners. We have focused this review on the connection between oxidative stress induction and the toxic effects of fetal and adult dioxin exposure, with emphasis on the large species difference in sensitivity to this agent. We examine the roles that the dioxin-inducible cytochromes P450s play in the cellular and toxicological consequences of dioxin exposure with emphasis on oxidative stress involvement. Many components of the health consequences resulting from dioxin exposure may be attributable to epigenetic mechanisms arising from prolonged reactive oxygen generation.

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“…Elevated serum lipids are a well-documented risk factor for atherosclerosis and ischemic heart disease. Furthermore, animal studies have shown that dioxin and coplanar PCBs cause the production of ROS (166,167), which in turn causes damage to endothelial cells and promotes the formation of foam cells and atherosclerotic plaques (168)(169)(170). These actions are similar to those caused by PAHs in tobacco smoke in human endothelial cells (171)…”

Section: Cardiovascular Diseasementioning

confidence: 98%

“…The combination of metal-induced oxidative stress with other mechanisms of toxicity induced by organic toxicants is of significant concern. In addition, a number of organic toxicants including TCDD, PCBs, and PAHs may also induce oxidative stress (167,(297)(298)(299). The effects of co-exposure to metals and organic toxicants may therefore be compounding.…”

Section: Heavy Metal-organic Toxicant Interactionsmentioning

confidence: 99%

Understanding the human health effects of chemical mixtures.

Carpenter

Arcaro

Spink

2002

Environ Health Perspect

323

198

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Most research on the effects of chemicals on biologic systems is conducted on one chemical at a time. However, in the real world people are exposed to mixtures, not single chemicals. Although various substances may have totally independent actions, in many cases two substances may act at the same site in ways that can be either additive or nonadditive. Many even more complex interactions may occur if two chemicals act at different but related targets. In the extreme case there may be synergistic effects, in which case the effects of two substances together are greater than the sum of either effect alone. In reality, most persons are exposed to many chemicals, not just one or two, and therefore the effects of a chemical mixture are extremely complex and may differ for each mixture depending on the chemical composition. This complexity is a major reason why mixtures have not been well studied. In this review we attempt to illustrate some of the principles and approaches that can be used to study effects of mixtures. By the nature of the state of the science, this discussion is more a presentation of what we do not know than of what we do know about mixtures. We approach the study of mixtures at three levels, using specific examples. First, we discuss several human diseases in relation to a variety of environmental agents believed to influence the development and progression of the disease. We present results of selected cellular and animal studies in which simple mixtures have been investigated. Finally, we discuss some of the effects of mixtures at a molecular level.

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Induction of Oxidative Stress in Brain Tissues of Mice after Subchronic Exposure to 2,3,7,8-Tetrachlorodibenzo-p-dioxin

Cited by 32 publications

References 37 publications

Analysis of plasma indices of redox homeostasis in dairy cows reared in polluted areas of Piedmont (northern Italy)

Analysis of plasma indices of redox homeostasis in dairy cows reared in polluted areas of Piedmont (northern Italy)

Induction of Oxidative Stress Responses by Dioxin and other Ligands of the Aryl Hydrocarbon Receptor

Understanding the human health effects of chemical mixtures.

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